Two well known species of human disease-causing herpes simplex viruses are herpes simplex virus type 1 (HSV-1) and its close cousin, herpes simplex virus type 2 (HSV-2), collectively HSV. At the molecular level, HSV-1 and HSV-2 share approximately 50% of their DNA. Both types infect the body's mucosal surfaces, usually the mouth or genitals, and then establish latency in the nervous system. For both HSV-1 and HSV-2 infections, at least two-thirds of infected people have no symptoms, or symptoms too mild to notice. However, both types can recur and spread even when no symptoms are present.
Moreover, prior infection with another STD, such as HSV 2, predisposes an individual to a higher risk of contracting HIV. In the U.S. alone, up to 25% of the population is seropositive for HSV 2. This figure rises to 80% in sub-Saharan Africa, where HIV is endemic. Viral reactivation of HSV occurs in >95% of healthy individuals and leads to the formation of genital ulcerations, resulting in destruction of the mucosal barrier and an influx of activated CD4+ T cells-optimal conditions for HIV infection. Therefore, decrease in HSV 2 infection could lead to a significant drop in HIV infection rates.
Since vaccines giving mucosal protection are probably many years away and condoms, although highly effective in preventing infection by sexually transmitted disease (STD) causing microbes, have failed to become generally accepted by males in many parts of the world, protective means are required which are under the control of the woman and can, if necessary, be used without the knowledge or consent of the male partner. Vaginal microbicides would meet this requirement and could not only protect the female's reproductive tract against infectious agents transmitted by the male, but could also protect the male's genital mucosa against possible infectious agents from the female.
Accordingly, it would be desirable to develop new treatments for viral diseases in general and STDs in particular that can be used frequently without adverse effects.